Positron emission tomographic imaging in stroke: Cross-sectional and follow-up assessment of amyloid in ischemic stroke

Ramesh Sahathevan, Thomas Linden, Victor L. Villemagne, Leonid Churilov, John V. Ly, Christopher Rowe, Geoffrey Donnan, Amy Brodtmann

Research output: Contribution to journalArticle

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Abstract

Background and Purpose - Cardiovascular risk factors significantly increase the risk of developing Alzheimer disease. A possible mechanism may be via ischemic infarction-driving amyloid deposition. We conducted a study to determine the presence of β-amyloid in infarct, peri-infarct, and hemispheric areas after stroke. We hypothesized that an infarct would trigger β-amyloid deposition, with deposition over time. Methods - Patients were recruited within 40 days of acute ischemic stroke and imaged with computed tomographic or magnetic resonance imaging and Pittsburgh compound B (11C-PiB) positron emission tomographic scans. Follow-up positron emission tomographic scanning was performed in a subgroup ≤18 months after the stroke event. Standardized uptake value ratios for regions of interest were analyzed after coregistration. Results - Forty-seven patients were imaged with 11C-PiB positron emission tomography. There was an increase in 11C-PiB accumulation in the stroke area compared with a reference region in the contralesional hemisphere, which was not statistically significant (median difference in standardized uptake value ratio, 0.07 [95% confidence interval, -0.06 to 0.123]; P=0.452). There was no significant increase in the accumulation of 11C-PiB in the peri-infarct region or in the ipsilesional hemisphere (median difference in standardized uptake value ratio, 0.04 [95% confidence interval, -0.02 to 0.10]; P=0.095). We repeated 11C-PiB positron emission tomography in 21 patients and found a significant reduction in accumulation of 11C-PiB between regions of interest (median difference in standardized uptake value ratio, -0.08 [95% confidence interval, -0.23 to -0.03]; P=0.04). Conclusions - There was no significant increase in 11C-PiB accumulation in or around the infarct. There was no increase in ipsilesional hemispheric 11C-PiB accumulation over time. We found no evidence that infarction leads to sustained or increased β-amyloid deposition ≤18 months after stroke.

Original languageEnglish
Pages (from-to)113-119
Number of pages7
JournalStroke
Volume47
Issue number1
DOIs
Publication statusPublished - 1 Jan 2016

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Amyloid
Stroke
Electrons
Confidence Intervals
Positron-Emission Tomography
Infarction
Alzheimer Disease
Magnetic Resonance Imaging

Keywords

  • Alzheimer disease
  • follow-up studies
  • positron emission tomography
  • risk factors

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Clinical Neurology
  • Advanced and Specialised Nursing

Cite this

Sahathevan, R., Linden, T., Villemagne, V. L., Churilov, L., Ly, J. V., Rowe, C., ... Brodtmann, A. (2016). Positron emission tomographic imaging in stroke: Cross-sectional and follow-up assessment of amyloid in ischemic stroke. Stroke, 47(1), 113-119. https://doi.org/10.1161/STROKEAHA.115.010528

Positron emission tomographic imaging in stroke : Cross-sectional and follow-up assessment of amyloid in ischemic stroke. / Sahathevan, Ramesh; Linden, Thomas; Villemagne, Victor L.; Churilov, Leonid; Ly, John V.; Rowe, Christopher; Donnan, Geoffrey; Brodtmann, Amy.

In: Stroke, Vol. 47, No. 1, 01.01.2016, p. 113-119.

Research output: Contribution to journalArticle

Sahathevan, R, Linden, T, Villemagne, VL, Churilov, L, Ly, JV, Rowe, C, Donnan, G & Brodtmann, A 2016, 'Positron emission tomographic imaging in stroke: Cross-sectional and follow-up assessment of amyloid in ischemic stroke', Stroke, vol. 47, no. 1, pp. 113-119. https://doi.org/10.1161/STROKEAHA.115.010528
Sahathevan, Ramesh ; Linden, Thomas ; Villemagne, Victor L. ; Churilov, Leonid ; Ly, John V. ; Rowe, Christopher ; Donnan, Geoffrey ; Brodtmann, Amy. / Positron emission tomographic imaging in stroke : Cross-sectional and follow-up assessment of amyloid in ischemic stroke. In: Stroke. 2016 ; Vol. 47, No. 1. pp. 113-119.
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AB - Background and Purpose - Cardiovascular risk factors significantly increase the risk of developing Alzheimer disease. A possible mechanism may be via ischemic infarction-driving amyloid deposition. We conducted a study to determine the presence of β-amyloid in infarct, peri-infarct, and hemispheric areas after stroke. We hypothesized that an infarct would trigger β-amyloid deposition, with deposition over time. Methods - Patients were recruited within 40 days of acute ischemic stroke and imaged with computed tomographic or magnetic resonance imaging and Pittsburgh compound B (11C-PiB) positron emission tomographic scans. Follow-up positron emission tomographic scanning was performed in a subgroup ≤18 months after the stroke event. Standardized uptake value ratios for regions of interest were analyzed after coregistration. Results - Forty-seven patients were imaged with 11C-PiB positron emission tomography. There was an increase in 11C-PiB accumulation in the stroke area compared with a reference region in the contralesional hemisphere, which was not statistically significant (median difference in standardized uptake value ratio, 0.07 [95% confidence interval, -0.06 to 0.123]; P=0.452). There was no significant increase in the accumulation of 11C-PiB in the peri-infarct region or in the ipsilesional hemisphere (median difference in standardized uptake value ratio, 0.04 [95% confidence interval, -0.02 to 0.10]; P=0.095). We repeated 11C-PiB positron emission tomography in 21 patients and found a significant reduction in accumulation of 11C-PiB between regions of interest (median difference in standardized uptake value ratio, -0.08 [95% confidence interval, -0.23 to -0.03]; P=0.04). Conclusions - There was no significant increase in 11C-PiB accumulation in or around the infarct. There was no increase in ipsilesional hemispheric 11C-PiB accumulation over time. We found no evidence that infarction leads to sustained or increased β-amyloid deposition ≤18 months after stroke.

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